Mannitol clearance for the determination of glomerular filtration rate–a validation against clearance of 51Cr‐EDTA

We studied the agreement between plasma clearance of mannitol and the reference method, plasma clearance of ⁵¹Cr‐EDTA in outpatients with normal to moderately impaired renal function. Forty‐one patients with a serum creatinine <200 μmol l^?1 entered the study. ⁵¹Cr‐EDTA clearance was measured with the standard bolus injection technique and glomerular filtration rate (GFR) was calculated by the single‐sample method described by Jacobsson. Mannitol, 0·25 g kg^?1 body weight (150 mg ml^?1), was infused for 4–14 min and blood samples taken at 1‐, 2‐, 3‐ and 4‐h (n = 24) or 2‐, 3‐, 3·5‐ and 4‐h after infusion (n = 17). Mannitol in serum was measured by an enzymatic method. Plasma clearance for mannitol and its apparent volume of distribution (Vd) were calculated according to Brøchner‐Mortensen. Mean plasma clearance (±SD) for ⁵¹Cr‐EDTA was 59·7 ± 18·8 ml min^?1. The mean plasma clearance for mannitol ranged between 57·0 ± 20·1 and 61·1 ± 16·7 ml min^?1 and Vd was 21·3 ± 6·2% per kg b.w. The between‐method bias ranged between ?0·23 and 2·73 ml min^?1, the percentage error between 26·7 and 39·5% and the limits of agreement between ?14·3/17·2 and ?25·3/19·9 ml min^?1. The best agreement was seen when three‐ or four‐sample measurements of plasma mannitol were obtained and when sampling started 60 min after injection. Furthermore, accuracy of plasma clearance determinations was 88–96% (P30) and 41–63% (P10) and was highest when three‐ or four‐sample measurements of plasma mannitol were obtained, including the first hour after the bolus dose. We conclude that there is a good agreement between plasma clearances of mannitol and ⁵¹Cr‐EDTA for the assessment of GFR.     

A comparison of single plasma sample methods to estimate renal clearance using 99mTc‐ethylenedicysteine and 99mTc‐mercaptoacetyltriglycine

Several single sample methods for determination of ^99mTc‐mercaptoacetyltriglycine (MAG3) clearance are being used clinically. Kabasakal et al. proposed a similar formula for ^99mTc‐ethylenedicysteine (EC). This study was performed to compare his method with Bubeck et al. formula for ^99mTc‐MAG3 already in use. Twenty‐eight subjects divided in two groups were registered which included 22 patients with various renal diseases (group‐I) and six normal volunteers (group II). All subjects were studied twice using both the radiopharmaceuticals. The images and renogram parameters, that is T_MAX and T_1/2 of both the agents, were similar in all the subjects. The clearance of the ^99mTc‐EC was however considerably higher than ^99mTc‐MAG3 in both the groups (mean ± SEM =279 ± 14 ml min^?1/1·73 m² versus 177 ± 15 ml min^?1/1·73 m² in group‐I and 377 ± 11·90 ml min^?1/1·73 m² versus 238 ± 8·23 ml min^?1/1·73 m² in group II). This difference was more pronounced in cases with reduced renal functions. Among the Effective Renal Plasma Flow (ERPF) values determined from EC and MAG3 clearances in six normal volunteers, four cases only in MAG3 had ERPF below the lower limit. This study has demonstrated superiority of single sample method for ^99 mTc‐EC clearance over its analogous method for ^99mTc‐MAG3.     

Restoration of peak vascular conductance after simulated microgravity by maximal exercise

We sought to determine if (i) peak vascular conductance of the calf was reduced following prolonged exposure to simulated microgravity, and (ii) if maximal cycle ergometry performed at the end of microgravity exposure stimulated a restoration of peak calf vascular conductance. To do this, peak vascular conductance of the calf was recorded following ischaemic plantar flexion exercise to fatigue in seven men after 16 days of head-down tilt (HDT) under two conditions: (i) after one bout of maximal supine cycle ergometry completed 24 h prior to performance of ischaemic plantar flexion exercise, and (ii) in a control (no cycle ergometry) condition. Following HDT, peak vascular conductance was reduced in the control condition (0·38 ± 0·02 to 0·24 ± 0·02 ml 100 ml^?1 min^?1 mmHg^?1; P = 0·04), but was restored when subjects performed cycle ergometry (0·33 ± 0·05 to 0·28 ± 0·04 ml 100 ml^?1 min^?1 mmHg^?1; P = 0·46). After HDT, time to fatigue during ischaemic plantar flexion exercise was not different from pre-HDT 24 h after performance of exhaustive cycle ergometry (120 ± 24 vs. 122 ± 19 s), but was decreased in the control condition (116 ± 11 vs. 95 ± 8 s; P = 0·07). These data suggest that a single bout of maximal exercise can provide a stimulus to restore peak vascular conductance and maintain time to fatigue during performance of ischaemic plantar flexion exercise.     

Anatomical vertebral artery hypoplasia and insufficiency impairs dynamic blood flow regulation

Recent studies have suggested that vertebral artery (VA) hypoplasia is a predisposing factor for posterior cerebral stroke. We examined whether anatomical vertebrobasilar ischemia, i.e., unilateral VA hypoplasia and insufficiency, impairs dynamic blood flow regulation. Twenty‐eight female subjects were divided into three groups by defined criteria: (i) unilateral VA hypoplasia (n = 8), (ii) VA insufficiency (n = 6), and (iii) control (n = 14). Hypoplastic VA criterion was VA blood flow of 40 ml min^?1, whereas VA insufficiency criterion was net (left + right) VA blood flow of 100 ml min^?1 or less. We evaluated left, right, and net VA blood flows by ultrasonography during hypercapnia, normocapnia, and hypocapnia to evaluate VA CO₂ reactivity. The unilateral VA hypoplasia group showed lower CO₂ reactivity at hypoplastic VA than at non‐hypoplastic VA (2·65 ± 0·58 versus 3·00 ± 0·48% per mmHg, P = 0·027) and net VA CO₂ reactivity was preserved (Unilateral VA hypoplasia, 2·95 ± 0·48 versus Control, 2·93 ± 0·42% per mmHg, P = 0·992). However, the VA insufficiency group showed a lower net VA CO₂ reactivity compared to the control (2·29 ± 0·55 versus 2·93 ± 0·42% per mmHg, P = 0·032) and the unilateral VA hypoplasia (P = 0·046). VA hypoplasia reduced CO₂ reactivity, although non‐hypoplastic VA may compensate this regulatory limitation. In subjects with VA insufficiency, lowered CO₂ reactivity at the both VA could not preserve normal net VA CO₂ reactivity. These findings provide a possible physiological mechanism for the increased risk of posterior cerebral stroke in subjects with VA hypoplasia and insufficiency.     

Calculation algorithms alter the breath‐by‐breath gas exchange values when abrupt changes in ventilation occur

The automatic metabolic units calculate breath‐by‐breath gas exchange from the expiratory data only, applying an algorithm (‘expiration‐only’ algorithm) that neglects the changes in the lung gas stores. These last are theoretically taken into account by a recently proposed algorithm, based on an alternative view of the respiratory cycle (‘alternative respiratory cycle’ algorithm). The performance of the two algorithms was investigated where changes in the lung gas stores were induced by abrupt increases in ventilation above the physiological demand. Oxygen, carbon dioxide fractions and ventilatory flow were recorded at the mouth in 15 healthy subjects during quiet breathing and during 20‐s hyperventilation manoeuvres performed at 5‐min intervals in resting conditions. Oxygen uptakes and carbon dioxide exhalations were calculated throughout the acquisition periods by the two algorithms. Average ventilation amounted to 6·1 ± 1·4 l min^?1 during quiet breathing and increased to 41·8 ± 27·2 l min^?1 during the manoeuvres (P<0·01). During quiet breathing, the two algorithms provided overlapping gas exchange data and noise. Conversely, during hyperventilation, the ‘alternative respiratory cycle’ algorithm provided significantly lower gas exchange data as compared to the values yielded by the ‘expiration‐only’ algorithm. For the first breath of hyperventilation, the average values provided by the two algorithms amounted to 0·37 ± 0·34 l min^?1 versus 0·96 ± 0·73 l min^?1 for O₂ uptake and 0·45 ± 0·36 l min^?1 versus 0·80 ± 0·58 l min^?1 for exhaled CO₂ (P<0·001 for both). When abrupt increases in ventilation occurred, such as those arising from a deep breath, the ‘alternative respiratory cycle’ algorithm was able to halve the artefactual gas exchange values as compared to the ‘expiration‐only’ approach.     

Gamma‐variate plasma clearance versus urinary plasma clearance of 51Cr‐EDTA in patients with cirrhosis with and without fluid retention

In patients with fluid retention, the plasma clearance of ⁵¹Cr‐EDTA (Cl_exp obtained by multiexponential fit) may overestimate the glomerular filtration rate (GFR). The present study was undertaken to compare a gamma‐variate plasma clearance (Cl_gv) with the urinary plasma clearance of ⁵¹Cr‐EDTA (Cl_u) in patients with cirrhosis with and without fluid retention. A total of 81 patients with cirrhosis (22 without fluid retention, 59 with ascites) received a quantitative intravenous injection of ⁵¹Cr‐EDTA followed by plasma and quantitative urinary samples for 5 h. Cl_gv was determined from the injected dose relative to the plasma concentration‐time area, obtained by a gamma‐variate iterative fit. Cl_exp and Cl_u were determined by standard technique. In patients without fluid retention, Cl_gv, Cl_exp and Cl_u were closely similar. The difference between Cl_gv and Cl_u (Cl_gv – Cl_u = ΔCl) was mean ?0·6 ml min^?1 1·73 m^?2. In patients with ascites, ΔCl was significantly higher (11·8 ml min^?1 1·73 m^?2, P<0·0001), but this value was lower than Cl_exp – Cl_u (17·5 mL min^?1 1·73 m^?2, P<0·01). ΔCl increased with lower values of GFR (P<0·001). In conclusion, in patients with fluid retention and ascites Cl_gv and Cl_exp overestimates GFR substantially, but the overestimation is smaller with Cl_gv. Although Cl_u may underestimate GFR slightly, patients with ascites should collect urine quantitatively to obtain a reliable measurement of GFR.     

Cholinergic blockade and the mesenteric artery response to head-up tilt-induced central hypovolaemia

The influence of muscarinic blockade on the superior mesenteric artery (SMA) response to head-up tilt (HUT) was assessed by Doppler ultrasound in eight healthy adults pretreated with i.v. glycopyrron. During supine rest, cholinergic blockade increased heart rate from 58 ± 3 to 106 ± 6 beats min^?1 (mean ± SE) and mean arterial pressure from 81 ± 3 to 97 ± 4 mmHg (P<0·01) and it reduced the cardiac stroke volume from 89 ± 6 to 59 ± 7 ml (P<0·01) with no significant effect on the SMA diameter and blood flow velocities. HUT provoked a further increase in heart rate to 134 ± 5 beats min^?1(P<0·01) and a reduction in stroke volume to 45 ± 4 ml (P<0·01). The early diastolic velocity increased from ?51 ± 4 to 6 ± 8 cm s^?1 during the normotensive stage of HUT and further to 21 ± 9 cm s^?1 during the hypotensive stage with a reduction in mean arterial pressure from 97 ± 4 to 73 ± 7 mmHg (P<0·01) but, in contrast to control HUT (without cholinergic blockade), the end-diastolic velocity did not change significantly. Maintenance of blood velocity and diameter in spite of an increase in arterial pressure at rest indicates increased SMA impedance. Likewise, during hypovolaemia, a glycopyrron-induced inhibition in diastolic velocity supports an increase in SMA impedance. The results indicate cholinergic vasorelaxing influence on the superior mesenteric artery both at rest and during normotensive central hypovolaemia.     

The associations between peak O2 consumption and leptin in 10‐ to 12‐year‐old boys

The aim of this study was to assess the associations of circulating levels of leptin with the peak O₂ consumption (VO_2peak) in 10 ‐ to 12‐year‐old boys of different BMI selected by Cole et al. (BMJ, 320,2000,1–6): total group (n = 248), normal (n = 190), overweight (n = 34) and obese (n = 24). We hypothesized that there is a close relationship in overweight and obese subgroups of boys with relative VO_{2peak kg}^?1(ml min^?1 kg^?1) and leptin. Most of the subjects were Tanner stage 2. Peak O₂ consumption was measured directly using an increasing incremental protocol until volitional exhaustion on an electronically braked cycle ergometer. The expired gas was sampled continuously breadth‐by‐breadth mode for the measurement of oxygen consumption (MetaMax, Germany). Blood samples were obtained after an overnight fast from an antecubital vein for leptin measurements. Peak O₂ consumption (l min^?1) was higher or lower (ml min^?1 kg^?1) in overweight and obese groups, compared with normal BMI group. Leptin was higher in overweight and obese groups, compared with normal BMI group. Peak O₂ consumption (l min^?1) correlated significantly with leptin only in total group (n = 248, r   =   0·196). Contrary, relative VO_2peak kg^?1 correlated significantly and negatively with leptin. The relationship was highest on the total group (r   =  ?0·674). We can conclude that leptin first of all correlated negatively with relative peak O₂ consumption. Absolute VO_2peak correlated with leptin only in total group.     

Simultaneous quantification of myocardial perfusion,oxidative metabolism,cardiac efficiency and pump function at rest and during supine bicycle exercise using 1‐11C‐acetate PET – a pilot study

Background: PET using 1‐¹¹C‐acetate (ACE‐PET) applied at rest is used for measuring absolute myocardial blood flow (MBF) and oxidative metabolic rate (k_mono). We evaluated the feasibility of quantitative ACE‐PET during exercise. Methods: Five endurance athletes underwent dynamic PET scanning at rest and during supine bicycle stress. Exercise was maintained at a workload of 120 Watt for 17 min. The rate‐pressure product (RPP) was recorded repeatedly. MBF, k_mono in left (LV) and right (RV) ventricular wall, cardiac output (CO), cardiac efficiency and a lung uptake value reflecting left heart diastolic pressures were calculated from the PET data using previously validated models. Results: MBF increased from 0·71 ± 0·17 to 2·48 ± 0·25 ml min^?1 per ml, LV‐k_mono from 0·050 ± 0·005 to 0·146 ± 0·021 min^?1, RV‐k_mono from 0·023 + 0·006 to 0·087 + 0·014 min^‐1, RPP from 4·7 ± 0·8 to 13·2 ± 1·4 mmHg × min^?1 × 10³ and Cardiac Output from 5·2 ± 1·1 to 12·3 ± 1·2 l min ^?1 (all P < 0·001). Cardiac efficiency was unchanged (P = 0·99). Lung uptake decreased from 1·1 ± 0·2 to 0·6 ± 0·1 ml g^?1 (P < 0·001). Discussion: A number of important parameters related to cardiac function can be quantified non‐invasively and simultaneously with a short scanning protocol during steady state supine bicycling. This might open up new opportunities for studies of the integrated cardiac physiology in health and early asymptomatic disease.     

The effects of exercise modality on the incidence of plateau at V·O2max

The purpose of this study was to determine the effect of exercise modality on the incidence of plateau at . Twelve recreationally active men (age, 21·7 ± 2·3 year; mass, 74·8 ± 6·5 kg; height, 177·6 ± 5·6 cm) completed four incremental tests to volitional exhaustion, of which two were completed on a treadmill (TRE) and two were completed using a cycle ergometer (CYC). The work rate employed for CYC was 1 W·2 s^?1 from an initial loading of 100 W with cadence being maintained at 60 rpm. For TRE, the workload (gradient) increased at a rate of 0·5% · 30 s^?1while maintaining a constant running speed of 10 kph. Throughout all the trials, was determined on a breath‐by‐breath basis using a precalibrated metabolic cart. The criteria adopted for determination of a plateau was a Δ over the final two consecutive 30‐s sampling periods of ≤50 ml · min^?1. Averaging across the two trials per each exercise modality showed a significant difference for plateau incidence between CYC (8%) and TRE (58%) (P = 0·017). This was aligned with a significant difference in the slope of the regression line during the final 60 s of the test, CYC (99·9 ± 49·7 ml · min^?1) and TRE (49·6 ± 42·6 ml · min^?1) (P = 0·017). Repeat measures ANOVA of these data suggests that plateau incidence rates at differ between treadmill‐ and cycle ergometry‐based exercises. Future studies need to address whether these response rates are replicated in well‐trained athletes.     

Mesenteric artery response to head-up tilt-induced centralhypovolaemia and hypotension

Superior mesenteric artery (SMA) blood flow and impedance were evaluated byduplex ultrasound during head-up tilt (HUT)-induced central hypovolaemia and hypotension ineight healthy volunteers. HUT induced a reduction in cardiac stroke volume from88·8±6·3 to 64·7±6·3 ml(mean±SEM; P<0·01) and an increase in thoracic electricimpedance from 38·6±2·1 to 42·6±2·1Ω (P<0·01) reflecting a reduced central blood volume. Maintainedtilt provoked a 30% reduction in mean arterial pressure (from 87·1±3·3to 63·4±3·6 mmHg; P<0·01) and the appearanceof presyncopal symptoms. During both the normotensive and the hypotensive phase of HUT, theSMA diameter (5·7±0·03 mm) and blood flow (514±75 ml min^?1) did not change significantly, although the end-diastolic velocity increasedfrom 9·7±4·8 to 39·7±4·0 cm s^?1 (P<0·01). The increase in diastolic velocity, despite amaintained or reduced arterial pressure, supports a reduction in the SMA impedance as it wasreproduced during a meal test when a moderate reduction in mean arterial pressure (87±4to 80±4 mmHg; P=0·04) was accompanied by a ninefoldincrease in the end-diastolic velocity (P<0·01). The results indicate areduction in the mesenteric vascular impedance to the extent that superior mesenteric artery bloodflow is maintained during HUT-induced central hypovolaemia and hypotension.     

Forearm metabolism during infusion of adrenaline: comparison of the dominant and non‐dominant arm

Human skeletal muscle metabolism is often investigated by measurements of substrate fluxes across the forearm. To evaluate whether the two forearms give the same metabolic information, nine healthy subjects were studied in the fasted state and during infusion of adrenaline. Both arms were catheterized in a cubital vein in the retrograde direction. A femoral artery was catheterized for blood sampling, and a femoral vein for infusion of adrenaline. Forearm blood flow was measured by venous occlusion strain‐gauge plethysmography. Forearm subcutaneous adipose tissue blood flow was measured by the local ¹³³Xe washout method. Metabolic fluxes were calculated as the product of forearm blood flow and a‐v differences of metabolite concentrations. After baseline measurements, adrenaline was infused at a rate of 0·3 nmol kg^?1 min^?1. No difference in the metabolic information obtained in the fasting state could be demonstrated. During infusion of adrenaline, blood flow and lactate output increased significantly more in the non‐dominant arm (8·12 ± 1·24 versus 6·45 ± 1·19 ml 100 g^?1 min^?1) and (2·99 ± 0·60 versus 1·83 ± 0·43 μmol 100 g^?1 min^?1). Adrenaline induced a significant increase in oxygen uptake in the non‐dominant forearm (baseline period: 4·98 ± 0·72 μmol 100 g^?1 min^?1; adrenaline period: 6·63 ± 0·62 μmol 100 g^?1 min^?1) while there was no increase in the dominant forearm (baseline period: 5·69 ± 1·03 μmol 100 g^?1 min^?1; adrenaline period: 4·94 ± 0·84 μmol 100 g^?1 min^?1). It is concluded that the two forearms do not respond equally to adrenaline stimulation. Thus, when comparing results from different studies, it is necessary to know which arm was examined.     

Inert gas rebreathing: the effect of haemoglobin based pulmonary shunt flow correction on the accuracy of cardiac output measurements in clinical practice

Background: Cardiac output (CO) is an important cardiac parameter, however its determination is difficult in clinical routine. Non‐invasive inert gas rebreathing (IGR) measurements yielded promising results in recent studies. It directly measures pulmonary blood flow (PBF) which equals CO in absence of significant pulmonary shunt flow (Q_S). A reliable shunt correction requiring the haemoglobin concentration (c_Hb) as only value to be entered manually has been implemented. Therefore, the aim of the study was to evaluate the effect of various approaches to Q_S correction on the accuracy of IGR. Methods: Cardiac output determined by cardiac magnetic resonance imaging (CMR) served as reference values. The data was analysed in four groups: PBF without correcting for Q_S (group A), shunt correction using the patients’ individual c_Hb values (group B), a fixed standard c_Hb of 14·0 g dl^?1 (group C) and a gender‐adapted standard c_Hb for male (15·0 g dl^?1) and female (13·5 g dl^?1) probands each (group D). Results: 147 patients were analysed. Mean CO_CMR was 5·2 ± 1·4 l min^?1, mean CO_IGR was 4·8 ± 1·3 l min^?1 in group A, 5·1 ± 1·3 in group B, 5·1 ± 1·3 l min^?1 in group C and 5·1 ± 1·4 l min^?1 in group D. The accuracy in group A (mean bias 0·5 ± 1·1 l min^?1) was significantly lower as compared to groups B, C and D (0·1 ± 1·1 l min^?1; P<0·01). Conclusion: IGR allows a reliable non‐invasive determination of CO. Since PBF significantly increased the measurement bias, shunt correction should always be applied. A fixed c_Hb of 14·0 g dl^?1 can be used for both genders if the exact c_Hb value is not known. Nevertheless, the individual value should be used if any possible.     

Twenty‐four hour variation in heart rate variability indices derived from fractional differintegration

Assuming that RR time‐series behave as a fractionally differintegrated Gaussian process, García‐González et al. (2003) recently proposed new indices for quantifying variability and structure in RR data. One of these was the ‘fractional noise quantifier’ (fnQ), measuring the departure of an RR time‐series from a monofractal structure (i.e. a measure of its multifractality). Sixty‐nine participants (aged = 34·5 ± 12·4 years, body mass index (BMI) = 23·9 ± 2·9 kg m^?2, maximal oxygen uptake rate (O_2peak) = 42·4 ± 10·9 ml min^?1 kg^?1, 39 males) provided continuous beat‐to‐beat ECG recordings for a 24‐h period. Fractional differintegration was used to quantify fnQ, and heart rate variability was calculated in the time domain. All variables were evaluated during consecutive 1‐h periods and also during four 6‐h blocks corresponding to morning, afternoon, evening and night periods. Apart from RR, circadian trends in all variables were independent of gender (P = 0·11–0·59). Apart from fnQ, all variables exhibited circadian variation (0·0005<P<0·012). Although fnQ was statistically uniform during the 24‐h period, it showed a trend towards elevated values during evening and night. The main finding of this study was that fnQ was elevated by around 10% during the evening and night, although this was not statistically significant. This suggests that the structure of RR time‐series in healthy individuals is most strongly ‘multifractal’ during evening and night periods. fnQ appears to be a plausible surrogate measure of multifractality in RR time‐series.     

Effects of different periods of hypoxic training on glucose metabolism and insulin sensitivity

This study examined the effects of different periods of hypoxic training on glucose metabolism. Sedentary subjects underwent hypoxic training (FiO₂ = 15·0%) for either 2 weeks (2‐week group; n = 11) or 4 weeks (4‐week group; n = 10). The 2‐week group conducted training sessions on 6 days week^?1 for 2 weeks, whereas the 4‐week group conducted training sessions on 3 days week^?1 for 4 weeks. Body fat mass or abdominal fat area did not change after training period in either group. VO_2max increased in both groups after training period (42 ± 2 versus 43 ± 2 ml min^?1 kg^?1 in 2‐week group, 41 ± 1 versus 42 ± 2 ml min^?1 kg^?1 in 4‐week group). Both groups showed a reduction in mean blood pressure after training period (92 ± 3 versus 90 ± 3 mmHg in 2‐week group, 91 ± 2 versus 87 ± 2 mmHg in 4‐week group, P≤0·05). No change was observed in blood glucose response after glucose ingestion after training period. However, area under the curve for serum insulin concentrations after glucose ingestion significantly decreased in only 4‐week group (6910 ± 763 versus 5812 ± 872 μIU ml^?1 120 min, P≤0·05). In conclusion, hypoxic training reduced blood pressure with independent on training duration. However, a longer period of hypoxic training led to greater improvements in insulin sensitivity compared with equivalent training over a shorter period, suggesting that hypoxic training programmes for more than 4 weeks might be more beneficial for improving insulin sensitivity.     

Validation of non‐invasive haemodynamic methods in patients with liver disease: the Finometer and the Task Force Monitor

Patients with advanced cirrhosis often present a hyperdynamic circulation characterized by a decrease in systolic and diastolic blood pressure (SBP and DBP), and an increase in heart rate (HR) and cardiac output (CO). Accurate assessment of the altered circulation can be performed invasively; however, due to the disadvantages of this approach, non‐invasive methods are warranted. The purpose of this study was to compare continuous non‐invasive measurements of haemodynamic variables by the Finometer and the Task Force Monitor with simultaneous invasive measurements. In 25 patients with cirrhosis, SBP, DBP and HR were measured non‐invasively and by femoral artery catheterization. CO was measured non‐invasively and by indicator dilution technique. The non‐invasive pressure monitoring was considered acceptable with a bias (accuracy) and a SD (precision) not exceeding 5 and 8 mmHg, respectively, as recommended by the Association for the Advancement of Medical Instrumentation. The accuracy and precision of the Finometer and the Task Force Monitor were as follows: SBP: ?3·6 ± 17·9 and ?8·9 ± 17·5 mmHg, respectively; DBP: 4·2 ± 9·6 and 1·9 ± 8·6 mmHg, respectively; HR: 2·0 ± 6·9 and 2·2 ± 6·2 bpm, respectively; and CO: 0·1 ± 1·6 and ?1·0 ± 2·0 L min^?1, respectively. The study demonstrates that the overall performances of the Finometer and the Task Force Monitor in estimating absolute values of SBP, DBP, HR and CO in patients with cirrhosis are not equivalent to the gold standard, but may have an acceptable performance with repeated measurements.     

Determination of baroreflex gain using auto-regressive moving-average analysis during spontaneous breathing

The heart rate component of the arterial baroreflex gain (BRG) was determined with auto-regressive moving-average (ARMA) analysis during each of spontaneous (SB) and random breathing (RB) protocols. Ten healthy subjects completed each breathing pattern on two different days in each of two different body positions, supine (SUP) and head-up tilt (HUT). The R–R interval, systolic arterial pressure (SAP) and instantaneous lung volume were recorded continuously. BRG was estimated from the ARMA impulse response relationship of R–R interval to SAP and from the spontaneous sequence method. The results indicated that both the ARMA and spontaneous sequence methods were reproducible (r=0·76 and r=0·85, respectively). As expected, BRG was significantly less in the HUT compared to SUP position for both ARMA (mean ± SEM; 3·5 ± 0·3 versus 11·2 ± 1·4 ms mmHg^–1; P<0·01) and spontaneous sequence analysis (10·3 ± 0·8 versus 31·5 ± 2·3 ms mmHg^–1; P<0·001). However, no significant difference was found between BRG during RB and SB protocols for either ARMA (7·9 ± 1·4 versus 6·7 ± 0·8 ms mmHg^–1; P=0·27) or spontaneous sequence methods (21·8 ± 2·7 versus 20·0 ± 2·1 ms mmHg^–1; P=0·24). BRG was correlated during RB and SB protocols (r=0·80; P<0·0001). ARMA and spontaneous BRG estimates were correlated (r=0·79; P<0·0001), with spontaneous sequence values being consistently larger (P<0·0001). In conclusion, we have shown that ARMA-derived BRG values are reproducible and that they can be determined during SB conditions, making the ARMA method appropriate for use in a wider range of patients.     

The exercise heart rate profile in master athletes compared to healthy controls

Endurance exercise protects the heart via effects on autonomic control of heart rate (HR); however, its effects on HR indices in healthy middle‐aged men are unclear. This study compared HR profiles, including resting HR, increase in HR during exercise and HR recovery after exercise, in middle‐aged athletes and controls. Fifty endurance‐trained athletes and 50 controls (all male; mean age, 48·7 ± 5·8 years) performed an incremental symptom‐limited exercise treadmill test. The electrocardiographic findings and HR profiles were evaluated. Maximal O₂ uptake (52·6 ± 7·0 versus 34·8 ± 4·5 ml kg^?1 min^?1; P<0·001) and the metabolic equivalent of task (15·4 ± 1·6 versus 12·2 ± 1·5; P<0·001) were significantly higher in athletes than in controls. Resting HR was significantly lower in athletes than in controls (62·8 ± 6·7 versus 74·0 ± 10·4 beats per minute (bpm), respectively; P<0·001). Athletes showed a greater increase in HR during exercise than controls (110·1 ± 11·0 versus 88·1 ± 15·4 bpm; P<0·001); however, there was no significant between‐group difference in HR recovery at 1 min after cessation of exercise (22·9 ± 5·6 versus 21·3 ± 6·7 bpm; P = 0·20). Additionally, athletes showed a lower incidence of premature ventricular contractions (PVCs) during exercise (0·0% versus 24·0%; P<0·001). Healthy middle‐aged men participating in regular endurance exercise showed more favourable exercise HR profiles and a lower incidence of PVCs during exercise than sedentary men. These results reflect the beneficial effect of endurance training on autonomic control of the heart.     

Head‐to‐head comparison between Actigraph 7164 and GT1M accelerometers in adolescents

We compared, head‐to‐head, the old generation Actigraph model 7164 with the new generation Actigraph GT1M accelerometer. A total of 15 randomly selected teenagers (eight girls and seven boys) were investigated. They performed a treadmill test wearing the two kinds of accelerometers around the waist simultaneously. The treadmill test consisted of three different levels of speed 4, 6 and 8 km h^?1 for four consecutive minutes. Accelerometer counts per 1 sec epoch for the Actigraph GT1M versus the Actigraph 7164 were at 4 km h^?1 21·6 ± 12·9 versus 26·5 ± 11·5 counts, at 6 km h^?1 56·0 ± 23·2 versus 62·9 ± 25·6 counts and at 8 km h^?1 142·6 ± 37·2 versus 156·4 ± 34·9 counts (P<0·01 for all levels of speed). Data from the old generation Actigraph 7164 and the new generation Actigraph GT1M accelerometers differ, where the Actigraph GT1M generates 10‐23% lower values. Correction equation for Actigraph GT1M was Actigraph 7164 = 5·2484 +  Actigraph GT1M counts × 1·0448. These results need to be taken into consideration when using these devices.     

Effects of walking with blood flow restriction on limb venous compliance in elderly subjects

Venous compliance declines with age and improves with chronic endurance exercise. KAATSU, an exercise combined with blood flow restriction (BFR), is a unique training method for promoting muscle hypertrophy and strength gains by using low‐intensity resistance exercises or walking. This method also induces pooling of venous blood in the legs. Therefore, we hypothesized that slow walking with BFR may affect limb venous compliance and examined the influence of 6 weeks of walking with BFR on venous compliance in older women. Sixteen women aged 59–78 years were partially randomized into either a slow walking with BFR group (n = 9, BFR walk group) or a non‐exercising control group (n = 7, control group). The BFR walk group performed 20‐min treadmill slow walking (67 m min^?1), 5 days per week for 6 weeks. Before (pre) and after (post) those 6 weeks, venous properties were assessed using strain gauge venous occlusion plethysmography. After 6 weeks, leg venous compliance increased significantly in the BFR walk group (pre: 0·0518 ± 0·0084, post: 0·0619 ± 0·0150 ml 100 ml^?1 mmHg^?1, P<0·05), and maximal venous outflow (MVO) at 80 mmHg also increased significantly after the BFR walk group trained for 6 weeks (pre: 55·3 ± 15·6, post: 67·1 ± 18·9 ml 100 ml^?1 min^?1, P<0·01), but no significant differences were observed in venous compliance and MVO in the control group. In addition, there was no significant change in arm compliance in the BFR walk group. In conclusion, this study provides the first evidence that 6 weeks of walking exercise with BFR may improve limb venous compliance in untrained elder female subjects.